Chlorotetracycline As An Indicator Of The Interaction Of Calcium With Brain Membrane Fractions

The fluorescence of chlorotetracycline (CTC) in the presence of synaptosomes isolated from sheep brain is selectively increased by Ca2+ under conditions in which Mg2+, Na+, K+, Li+ or choline have only a small effect. The monovalent cations release bound Ca2+ from synaptosomes, and this effect is reflected by a decrease in the CTC fluorescence. Under optimal conditions there is a near parallelism between Ca2+ and CTC binding to the synaptosomes membranes, and Li+ is the monovalent cation tested which interferes the most with the binding of both substances. These results obtained in a predominantly sucrose medium become less distinct when media simulating physiological composition are utilized, which limits the usefulness of the method. Brain mitochondria and myelin also bind Ca2+ and CTC. The ratio of the fluorescence signal (or CTC bound) to Ca2+ bound is highest of all for mitochondrial membranes, and the apparent fluorescence quantum yield of CTC is also the highest in these membranes, which suggests that the Ca2+ in these membranes is localized in a more apolar region than is the case for synaptosomes and myelin

Reduction of EEG Theta Power and Changes in Motor Activity in Rats Treated with Ceftriaxone

The glutamate transporter GLT-1 is responsible for the largest proportion of total glutamate transport. Recently, it has been demonstrated that ceftriaxone (CEF) robustly increases GLT-1 expression. In addition, physiological studies have shown that GLT-1 up-regulation strongly affects synaptic plasticity, and leads to an impairment of the prepulse inhibition, a simple form of information processing, thus suggesting that GLT-1 over-expression may lead to dysfunctions of large populations of neurons. To test this possibility, we assessed whether CEF affects cortical electrical activity by using chronic electroencephalographic (EEG) recordings in male WKY rats. Spectral analysis showed that 8 days of CEF treatment resulted in a delayed reduction in EEG theta power (7–9 Hz) in both frontal and parietal derivations. This decrease peaked at day 10, i.e., 2 days after the end of treatment, and disappeared by day 16. In addition, we found that the same CEF treatment increased motor activity, especially when EEG changes are more prominent. Taken together, these data indicate that GLT-1 up-regulation, by modulating glutamatergic transmission, impairs the activity of widespread neural circuits. In addition, the increased motor activity and prepulse inhibition alterations previously described suggest that neural circuits involved in sensorimotor control are particularly sensitive to GLT-1 up-regulation